F0305
Anti-FANCD2 antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
Synonym(s):
Anti-FA4, Anti-FACD Fanconi Pancytopenia, type 4, Anti-FANCD, Anti-Fanconi Anemia, complementation group D
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About This Item
MDL number:
UNSPSC Code:
12352203
biological source
rabbit
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 170 kDa (doublet)
species reactivity
human
packaging
antibody small pack of 25 μL
technique(s)
indirect immunofluorescence: 1:250-1:500 using HEK 293T cells fixed with paraformaldehyde-Triton
microarray: suitable
western blot: 1:2,000-1:4,000 using extracts of the U2OS cell line
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
Gene Information
human ... FANCD2(2177)
Immunogen
synthetic peptide corresponding to amino acids 1-18 of human FANCD2, conjugated to KLH via a C-terminal added cysteine residue. The immunizing peptide is present in isoforms a and b of FANCD2.
Application
Anti-FANCD2 antibody produced in rabbit is suitable for the following applications:
- Indirect immunofluorescence at a dilution of 1:250-1:500 using HEK 293T cells fixed with paraformaldehyde-Triton
- Microarray
- Western blotting at a dilution of 1:2,000-1:4,000 using extracts of the U2OS cell line
Biochem/physiol Actions
Fanconi anemia group D2 protein is a protein encoded by the FANCD2 gene in humans. It is essential for proper cell cycle progression through mitosis and for the completion of cell division. FANCD2 may be aasociated with cell-death mechanism. It is necessary for the maintenance of genome stability during cell proliferation and is an effector of ATR signaling that is necessary for sustaining cell proliferation and attenuating carcinogenesis. Fanconi Anemia (FA) signaling pathway is a result from an inactivated FANCD2 and possesses a novel mechanism of modulating DNA damage response and repair. Fanconi anaemia (FA) is an autosomal recessive disorder and is characterized by pancytopenia, short stature, radial ray defects, skin hyperpigmentation and a predisposition to cancer.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Andreja Leskovac et al.
International journal of radiation biology, 90(5), 373-381 (2014-02-12)
As the Fanconi anemia (FA) pathway is required for appropriate cell cycle progression through mitosis and the completion of cell division, the aim of the present study was to determine the destiny of FA cells after irradiation in vitro and
Changxian Shen et al.
Cancer research, 73(11), 3393-3401 (2013-05-02)
Deregulation of the mTOR pathway is closely associated with tumorigenesis. Accordingly, mTOR inhibitors such as rapamycin and mTOR-selective kinase inhibitors have been tested as cancer therapeutic agents. Inhibition of mTOR results in sensitization to DNA-damaging agents; however, the molecular mechanism
Gérald Lossaint et al.
Molecular cell, 51(5), 678-690 (2013-09-03)
Proteins disabled in Fanconi anemia (FA) are necessary for the maintenance of genome stability during cell proliferation. Upon replication stress signaling by ATR, the FA core complex monoubiquitinates FANCD2 and FANCI in order to activate DNA repair. Here, we identified
M Whitney et al.
Nature genetics, 11(3), 341-343 (1995-11-01)
Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopenia, short stature, radial ray defects, skin hyperpigmentation and a predisposition to cancer. Cells from FA patients are hypersensitive to cell killing and chromosome breakage induced by DNA cross-linking
Jayabal Panneerselvam et al.
Oncotarget, 4(9), 1416-1426 (2013-08-24)
A compromised Fanconi Anemia (FA) signaling pathway, often resulting from an inactivated FANCD2, was recently recognized to contribute to the development of non-FA human tumors. However, it is largely unknown as to how an impaired FA pathway or an inactivated
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